Severe anterograde amnesia in patients and monkeys is known to result from damage to medial temporal lobe structures and the hippocampus has been shown to be the critical structure in the defect. Amnesia can also result from disease, or injury, of the diencephalon and damage to the medial dorsal thalamic nucleus and mammillary bodies is implicated in this form of amnesia. However, a) It is not clear whether damage to one or both structures is required to disrupt memory b) The equivalence of memory disorders in temporal lobe and diencephalic amnesia is being questioned by recent clinical and experimental findings which are taken to indicate tht rapid rates of forgetting are characteristic only of temporal lobe, but not of diencephalic, amnesia c) Accumulating evidence reveals that despite their amnesia, patients and experimental monkeys can learn, and retain, certain perceptual and cognitive tasks presented with repeated trials. This suggests the existence of a neural system capable of mediating learning in the absence of memory systems and, for several reasons, the neostriatum may constitute part of such a system. Our aims are: 1) To assess in the non-human primate the effects of separate, and combined, circumcribed lesions of medial dorsal thalamic nucleus and mammillary bodies on memory tasks that are sensitive to hippocampal damage, such as the delayed non-matching to sample recognition task, in both visual and tactual modalities. 2) To compare the rates of forgetting of monkeys with diencephalic lesions and those with hippocampal ablations by testing retention of a recognition task 1- and 24- hours after acquisition. 3) To test the notion that striatal damage will impair cumulative learing of tasks presented with repeated trials but not the rapid memorization of single-trial events. To this end, we will make lesions of either the tail of the caudate, or ventral putamen, and assess performance on a concurrent discrimination task under conditions of distributed practice and on a trial-unique recognition memory task. We expect monkeys with either type of striatal lesions to be impaired on the first, but not on the second, task and, conversely, we expect monkeys with hippocampal ablations to be impaired on the recognition memory task, but not on the concurrent discrimination task under conditions of distributed practice.